Science Briefs

Selected science news

[sciencebriefs]

Evolution of bacterial DNA appears to be sped up by the position of specific genes along the route of expected collisions between DNA-reading enzymes. Certain genes are in prime collision paths for the moving molecular machineries that read the DNA code. Replication (the duplicating of the genetic code prior to cell division) and transcription (the copying of DNA code to produce a protein) are not separated by time or space in bacteria. So clashes between the associated molecular machines are inevitable. Replication traveling rapidly along a DNA strand can be stalled by a head-on encounter or same-direction brush with slower-moving transcription. The researchers are trying to understand the evolutionary consequences of these conflicts in the model organism Bacillus subtilis. The major focus is on understanding mechanistic and physiological aspects of conflicts in living cells – including why and how these collisions lead to mutations. Impediments to replication can cause instability within the genome, such as chromosome deletions or rearrangements, or incomplete separation of genetic material during cell division. To avoid unwanted encounters, the majority of bacterial genes are oriented along the leading strand of DNA, rather than the lagging strand. The terms refer to the direction the encoding activities travel on different forks of the unwinding DNA. Head-on collisions between replication and transcription happen on the lagging strand. Despite the heightened risk of gene-altering clashes, in B. subtilis 25% of all its genes, and 6% of its essential genes, are oriented on the lagging strand. The scientists observed that genes under the greatest natural selection pressure for mutations, a sign of their adaptive significance, were on the lagging strand. Based on their analysis of mutations on the leading and the lagging strands, the researchers found that the rate of accumulation of mutations was faster in the genes oriented to be subject to head-on replication-transcription conflicts, in contrast to co-directional conflicts. According to the researchers, the mutational analyses of the genomes and the experimental findings together indicate that head-on conflicts were more likely than same-direction conflicts to cause mutations. They also found that longer genes provided more opportunities for replication-transcription conflicts to occur, so lengthy genes were more likely to mutate. More: • Head-on collisions of proteins create mutations

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Researchers have discovered more about how a stem cell’s environment influences what type of cell a stem cell will become. They have shown that whether human mesenchymal stem cells turn into fat or bone cells depends partially on how well they can grip the material they are growing in. Much research has been done on how stem cells grow on two-dimensional substrates, but comparatively little work has been done in three dimensions. Three-dimensional matrices for stems cells have mostly been treated as simple scaffolding, rather than as a signal that influences the cells’ development. Jason Burdick and his colleagues were interested in how these three-dimensional matrices impact mechanotransduction – how the cell takes information about its physical environment and translates that to chemical signaling. The researchers cultured mesenchymal stem cells in hydrogels – water-swollen polymer networks – which share some similarities with the environments stem cells naturally grow in. These materials are generally soft and flexible but can vary in density and stiffness depending on the type and quantity of the bonds between the polymers. In this case, the researchers used covalently cross-linked gels, which contain irreversible chemical bonds. When seeded on top of two-dimensional covalently cross-linked gels, mesenchymal stem cells spread and pulled on the material differently depending on how stiff it was. Critically, the mechanics guide cell fate, or the type of cells they differentiate it into. A softer environment would produce more fat-like cells and a stiffer environment, where the cells can pull on the gel harder, would produce more bone-like cells. However, when the researchers put mesenchymal stem cells inside three-dimensional hydrogels of varying stiffness, they didn’t see these kinds of changes. “In most covalently cross-linked gels, the cells can’t spread into the matrix because they can’t degrade the bonds — they all become fat cells,” Burdick said. “That tells us that in 3D covalent gels the cells don’t translate the mechanical information the same way they do in a 2D system.” To test this, the researchers changed the chemistry of their hydrogels so that the polymer chains were connected by a peptide that the cells could naturally degrade. They hypothesized that, as the cells spread, they would be able to get a better grip on their surrounding environment and thus be more likely to turn into bone-like cells. The results showed that the stem cells’ differentiation into bone-like cells was aided by their ability to better anchor themselves into the growth environment.

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It's hard for astronomers to understand how stars 10 times as massive as the Sun, or more, can exist, because as they grow, they tend to push away the gas they feed on, starving their own growth. Now researchers suggest that newly-formed stars may grow to great mass if they form within a group of older stars, if these surrounding stars are favorably arranged to confine and feed gas to the younger ones. The astronomers have seen evidence of this collective feeding, which they label “convergent constructive feedback”, in a giant cloud of gas and dust – Westerhout 3 (W3) – located 6,500 light years from us. To study the formation of high-mass stars, Alana Rivera-Ingraham and collaborators used far-infrared images from the European Space Agency's Herschel Space Observatory. Regions of the gas cloud where stars are about to form can be found by mapping the density of dust and its temperature, looking for the most dense regions where the dust is shielded and cold. Stars are born in the denser parts of gas clouds, where the gas gets compressed enough by gravity to trigger nuclear fusion. The more massive the newborn star, the more visible and ultraviolet light it emits, heating up its surroundings — including the dust studied by Herschel. However, “The radiation during the birth of high-mass stars is so intense that it tends to destroy and push away the material from which they need to feed for further growth,” explained Rivera-Ingraham. Scientists have modeled this process and found that stars about eight times the mass of our Sun would stop growing because they run out of gas. Yet astronomers do see stars that are more massive than this theoretical limit. The researchers noticed that the densest region of the cloud was surrounded by a group of old high-mass stars. Previous generations of large stars may enable the next ones to grow also massive, and close to each other. Like young high-mass stars, older stars also radiate and push gas away. If such older stars happen to be arranged favorably around a major reservoir of gas, they can compress it enough to ignite new stars. This corralling of dense gas can give birth to new, high-mass stars. A large newborn star will push its food source away, but if it is surrounded by enough large stars, these can keep nudging gas back at it. More: • Hunting high-mass stars with Herschel • Massive stars built in stellar nurseries

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Biologists have thought that new genes appear when evolution copies existing genes and then adapts the copies to new tasks. However, a recent study shows that new genes often form from scratch. Analysis of genes from mice, humans and fish shows that new genes are shorter than old ones and simpler in structure. These and other differences between young and old genes indicate that completely new genes can also form from previously unread regions of the genome. Moreover, the new genes often use existing regulatory elements from other genes before they create their own. The study found many exceptions to the previous belief. The researchers analysed over 20,000 mouse genes and traced their origins. According to their findings, genes that appeared later in evolution are often shorter than those that have been in existence longer. Moreover, younger genes have fewer exons and fewer protein domains. A new gene needs time to acquire additional exons and introns. So genes become longer with time and consist of numerous exons and introns. Analyses of human, zebrafish and stickleback genes confirm the correlations discovered in the mouse. The researchers also studied another way in which new genes can arise from existing genes: through a change in the reading frame. The genetic reading frame is a triplet of nucleotides. Each of these triplets corresponds, by the genetic code, to an amino acid. If this reading frame is shifted, subsequent triplets correspond to completely different amino acids. About 60% of modern genes originate from genes of early unicellular ancestors. Many new genes appeared during the advent of fundamental evolutionary innovations, such as the transition from unicellular to multicellular organisms and the emergence of vertebrates. However, the researchers only found a few locations on chromosomes in which newly formed genes accumulate. Instead, new genes are relatively evenly distributed across the entire genome. One of the few exceptions is a cluster of genes on chromosome 14 which control the activity of neurons, among other things. New genes thus frequently arise from scratch in the course of evolution, forming in the gene-free sections of the genome. Yet this often requires only minimal changes. “For example, genes need elements known as promoters which control their activity. It appears that new genes can appropriate promoters belonging to other genes and use them for their own purposes,” explained researcher Diethard Tautz.

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Scientists have discovered that a type of DNA damage – a double-strand break (DSB) – long thought to be detrimental to brain cells can actually be part of a regular, non-harmful process. The team further found that disruptions to this process occur in mouse models of Alzheimer's disease – and identified two therapeutic strategies that reduce these disruptions. DSB DNA damage has been considered a major cause of age-related diseases such as Alzheimer's. Now researchers report that DSBs in neurons in the brain can also be part of normal brain functions such as learning – as long as the DSBs are tightly controlled and repaired in good time. Further, the accumulation of the amyloid-beta protein in the brain – widely thought to be a major cause of Alzheimer's disease – increases the number of neurons with DSBs and delays their repair. In laboratory experiments, two groups of mice explored a new environment filled with unfamiliar sights, smells and textures. One group was genetically modified to simulate key aspects of Alzheimer's, and the other was a healthy, control group. As the mice explored, their neurons became stimulated as they processed new information. After the mice were returned to their home environment the investigators examined the neurons of the mice for markers of DSBs. The control group showed an increase in DSBs right after they explored the new environment – but after being returned to their home environment, DSB levels dropped. The group of mice modified to simulate Alzheimer's had higher DSB levels at the start – levels that rose even higher during neuronal stimulation. In addition, the team noticed a substantial delay in the DNA-repair process. To counteract the accumulation of DSBs, the team first used a therapeutic approach built on recent studies that showed the anti-epileptic drug levetiracetam could improve neuronal communication and memory in both mouse models of Alzheimer's and in humans in the disease's earliest stages. The mice they treated with the drug had fewer DSBs. In their second strategy, they genetically modified mice to lack the brain protein tau – also implicated in Alzheimer's. This manipulation also prevented the excessive accumulation of DSBs. More: • Brain Activity Breaks DNA • Learning hurts your brain

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Every time a cell divides it makes a copy of crucial ingredients, including the histone proteins that are responsible for spooling DNA into tight little coils around complexes of histone proteins ("nucleosomes"). When the histones aren’t made correctly, genomic instability can result. Seven years ago, researchers noticed an aggregation of proteins along a block of genome that codes for the critical histones, but they had no idea how this aggregate – a “histone locus body” (HLB) – was formed. Now, research conducted in fruit flies has identified a specific DNA sequence that both triggers the formation of the HLB and turns on all the histone genes in the entire block. The finding provides a model for the coordinated synthesis of histones needed for assembly into chromatin, a process critical to keeping chromosomes intact. “Our study has uncovered a new relationship between nuclear architecture and gene activity,” said senior study author Bob Duronio. “In order to make chromosomes properly, you need to make these histone building blocks at the right time and in the right amount. We found that the cell has evolved this complex architecture to do that properly, and that involves an interface between the assembly of various components and the turning on of a number of genes.” In the fruit fly, as in the human, the five different histone genes exist in one long chunk of the genome; the “histone locus”. In flies it contains 100 copies of each of the five genes, encompassing approximately 500,000 nucleotides. The proteins required for making the histone message – a process that must happen every time a new strand of DNA is copied – come together at this histone locus to form the HLB. The researchers wanted to figure out how these factors knew to meet at the histone locus. They inserted different combinations of the five histone genes into another site of the genome, and looked to see which combinations recruited a new HLB. They found that combinations that contained a specific 300 nucleotide sequence – the region between the H3 and H4 histone genes – formed a HLB. In contrast, combinations of genes that lacked this sequence did not form the body. They went on to show that this sequence turned on not only the H3 and H4 genes in its direct vicinity, but also other histone genes in the block.

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Cells in the body need to be acutely aware of their surroundings. A signal from one direction may cause a cell to react in a very different way than if it had come from another direction. Unfortunately, such vital directional cues are lost when cells are removed from their natural environment. Now, researchers have devised a way to mimic in the laboratory the spatially oriented signaling that cells normally experience. Using the technique, they’ve found that the location of a “divide now” signal on the membrane of a mouse embryonic stem cell governs where in that cell the plane of division occurs. It also determines which of two daughter cells remains a stem cell and which will become a progenitor cell to replace or repair damaged tissue. In the study, the effect on mouse embryonic stem cells of the protein Wnt3a – which is known to play a critical role in embryonic development and in the growth and maintenance of stem cells – was tested. Stem cells have many receptors for Wnt proteins on their surfaces, and Wnt3a has been shown to promote self-renewal over differentiation in several types of stem cells. Molecules of Wnt3a were attached to tiny synthetic beads, which were incubated with embryonic stem cells. The reaction over time of the cells to which a single bead-bound protein had attached via one of the cell’s many Wnt3a receptors was then observed. The effect of the localized signal was clear. In 75 percent of cases, the stem cell began to divide in a very specific orientation, with the plane of division occurring perpendicularly to the location of the incoming signal. In contrast, only 12 percent of cells exposed to beads bound to a control protein exhibited similar patterns of division. Also, the daughter cell closest to the Wnt3a signal expressed proteins showing it was maintaining its pluripotency. The one farthest from the signal, however, expressed proteins indicating that it was beginning to differentiate. The researchers speculate that the reduction in the intensity of the Wnt signal in the distant daughter cell is what causes it to begin the differentiation process; the loss of the Wnt3a signal is known to cause cultured stem cells to begin differentiating.

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Brown fat cells, as distinct from white fat cells, make heat for the body, and are thought to help mammals cope with the cold. But their role in generating warmth might also be applied to coping with obesity and diabetes. They are thought to counteract obesity by burning excess energy stored in lipid, while white fat cells store energy. Brown fat cells contain many smaller droplets of lipids and the most mitochondria (containing pigmented cytochromes that bind iron) of any cell type, which make them brown. Researchers have now found that a protein switch – early B cell factor-2 (Ebf2) – determines which developmental path fat precursor cells take – the brown or white cell trajectory. The team showed that Ebf2 regulates the binding activity of PPAR-γ, a protein that regulates differentiation of developing cell types and is the target of anti-diabetic drugs. Ebf2 affects PPAR-γ’s ability to determine if precursor cells follow the white or brown fat cell path. The team surmises that Ebf2 may alter epigenetic proteins at brown fat genes to expose PPAR-γ binding sites. Sona Rajakumari conducted a genome-wide study of PPAR-γ binding regions in white and brown fat cells. She found that brown cell-specific binding sites also contained a DNA-recognition site for Ebf2 transcription factors and that Ebf2 was strongly expressed in brown fat cells only. When she overexpressed Ebf2 in precursor white fat cells they matured into brown fat cells. The brown fat cell status of the reprogrammed white fat cells was confirmed in that they consumed greater amounts of oxygen (a surrogate measure of heat production), had a greater number of mitochondria, and had an increased expression of genes involved in heat production, all characteristics of normal brown fat cells. Rajakumari also looked at whether Ebf2 was required for brown fat cell development in animals by studying mice in which Ebf2 had been knocked out. She found that in late-stage embryos of these knockouts, white fat cells took the place of where brown fat cell reserves were in normal mice, indicating that stem cells differentiate into white fat in the absence of Ebf2. Ebf2 is the earliest known protein in the timeline of the development and differentiation of brown fat cells.

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Scientists have discovered that key gene regulators work in pairs to trigger stem cells to differentiate into specific cell types. Furthermore, they showed that selective partnering of the regulators result in uniquely specified developmental outcomes – it takes a pair of transcription factors, working tightly together, to orchestrate key decisions in embryo development. The study established that the transcription factor Oct4 alternatively partners with two related factors, Sox2 or Sox17. Such selective partnering of the two transcription factors can lead to very different developmental outcomes. Co-lead author Prasanna Kolatkar said, “Our previous work described how re-engineering of developmental proteins through a single site change results in functions of proteins Sox2 and Sox17 becoming inter-converted – thus the decision to stay as a stem cell or differentiate is flipped through a single amino acid change. This study uses a genome-wide approach to validate this concept, and moreover leads to novel genes potentially involved in primitive endoderm formation.” According to the research institute's executive director Huck Hui,"This work identified a novel regulatory switch from pluripotency to cell-lineage specific differentiation. It is remarkable that a single pluripotency factor, Oct4, was found to influence diverse cellular processes. This key discovery illustrates the complexity in the regulation of pluripotency programme in embryonic stem cells."

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Observations with the Atacama Large Millimeter/submillimeter Array (ALMA) show that the most vigorous bursts of star birth in the universe occurred much earlier than previously thought. The most intense bursts of star birth are thought to have occurred in the early universe, in massive, bright galaxies. These starburst galaxies convert vast reservoirs of cosmic gas and dust into new stars very rapidly — many hundreds of times faster than in spiral galaxies like the Milky Way. The international team of researchers first discovered these distant starburst galaxies with the 10-meter South Pole Telescope (SPT) and then used ALMA to examine them in more detail. They were surprised to find that many of these distant, dusty, star-forming galaxies are even further away than expected. So on average their bursts of star birth took place when the universe was just under 2 billion years old — a full billion years earlier than previously thought. Two of these galaxies are the most distant of their kind ever seen — so they are seen at a time the universe was only one billion years old. The team used ALMA to capture light from 26 of these galaxies at wavelengths of around three millimeters. Astronomers took advantage of gravitational lensing, an effect predicted by the general theory of relativity, where light from a distant galaxy is distorted by the gravitational influence of a nearer foreground galaxy, which acts like a lens and makes the distant source appear brighter. To understand how much this gravitational lensing brightened the view of the galaxies, the team made sharper images of them using more ALMA observations at wavelengths of around 0.9 millimeters. Analysis of the gravitational lensing distortion shows that some of the distant star-forming galaxies are as bright as 40 trillion Suns, and that gravitational lensing has magnified this by up to 22 times. “Only a few gravitationally lensed galaxies have been found before at these submillimeter wavelengths, but now SPT and ALMA have uncovered dozens of them.” said team member Carlos De Breuck. More: • ALMA finds 'monster' starburst galaxies in the early universe • Ancient, highly active galaxies discovered • ALMA exposes hidden star factories in the early universe • 'Nuisance' data lead to surprising star-birth discovery • Bursts of star formation in the early universe • NSF-funded Telescopes in Antarctica and Chile Discover Bursts of Star Formation in the Early Universe • Gravitational lensing - and a new telescope - reveal ancient starbursts • Witnessing Starbursts in Young Galaxies

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A team of sleep researchers has confirmed the mechanism that enables the brain to consolidate memory and found that a commonly prescribed sleep aid enhances the process. Earlier research found a correlation between sleep spindles — bursts of brain activity that last for a second or less during a specific stage of sleep — and consolidation of memories that depend on the hippocampus. The hippocampus, part of the cerebral cortex, is important in the consolidation of information from short-term to long-term memory, and spatial navigation. The team demonstrated the critical role that sleep spindles play in consolidating memory in the hippocampus, and they showed that pharmaceuticals could significantly improve that process, far more than sleep alone. “We found that a very common sleep drug can be used to increase verbal memory,” said team leader Sara Mednick. “This is the first study to show you can manipulate sleep to improve memory. It suggests sleep drugs could be a powerful tool to tailor sleep to particular memory disorders.” A total of 49 men and women between the ages of 18 and 39 who were normal sleepers were given varying doses of zolpidem (Ambien) or sodium oxybate (Xyrem), and a placebo. Researchers monitored their sleep, measured sleepiness and mood after napping, and used several tests to evaluate their memory. The researchers found that zolpidem significantly increased the density of sleep spindles and improved verbal memory consolidation. “(P)harmacologically enhancing sleep spindles in healthy adults produces exceptional memory performance beyond that seen with sleep alone or sleep with the comparison drug (sodium oxybate),” the researchers wrote. “… The results set the stage for targeted treatment of memory impairments as well as the possibility of exceptional memory improvement above that of a normal sleep period.”

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The flip of a single molecular switch helps create the mature neuronal connections that allow the brain to bridge the gap between adolescent impressionability and adult stability. Now researchers have reversed the process, recreating a youthful brain that facilitated both learning and healing in adult mice. It's long been known that the young and old brains are very different. Adolescent brains are more malleable or plastic, which allows them to learn languages more quickly than adults and speeds recovery from brain injuries. The comparative rigidity of the adult brain results in part from the function of a single gene that slows the rapid change in synaptic connections between neurons. By monitoring the synapses in living mice over weeks and months, researchers have identified the key genetic switch for brain maturation. The Nogo Receptor 1 gene is required to suppress high levels of plasticity in the adolescent brain and create the relatively quiescent levels of plasticity in adulthood. In mice without this gene, juvenile levels of brain plasticity persist throughout adulthood. When researchers blocked the function of this gene in old mice, they reset the old brain to adolescent levels of plasticity. “These are the molecules the brain needs for the transition from adolescence to adulthood,” said Stephen Strittmatter. senior author of the paper. “It suggests we can turn back the clock in the adult brain and recover from trauma the way kids recover.” Rehabilitation after brain injuries like strokes requires that patients re-learn tasks such as moving a hand. Researchers found that adult mice lacking Nogo Receptor recovered from injury as quickly as adolescent mice and mastered new, complex motor tasks more quickly than adults with the receptor. Researchers also showed that Nogo Receptor slows loss of memories. Mice without Nogo receptor lost stressful memories more quickly.

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Glial cells – a family of cells found in the human central nervous system and, until recently, considered mere housekeepers – now appear to promote the unique complexity of the human brain. This conclusion followed from a finding that when human astrocytes (a subtype of glia) were transplanted into mice they could improve communication in the brain, allowing the mice to learn more rapidly. Astrocytes are far more abundant, larger, and diverse in human brain than in other species. In humans, individual astrocytes project scores of fibers that can simultaneously connect with large numbers of neurons. So individual human astrocytes can potentially coordinate the activity of thousands of synapses. This suggested that human astrocytes might play a significant role in integrating and coordinating the more complex signaling activity found in human brains, and hence help regulate higher cognitive functions. This in turn suggested that, when transplanted into mice, human glia may influence underlying patterns of neural activity. The research team studied what happened when these cells were allowed to co-exist with the normal nerve cells of mice. They first isolated human glial progenitors, which give rise to astrocytes, from brain tissue. They then transplanted these into the brains of neonatal mice. As the mice matured, the human glial cells outcompeted the host’s native glia, while at the same time leaving the existing neural network intact. The team then examined the functional impact that these cells had on the animals’ brains, specifically the speed and retention of signals between cells in the brain and its plasticity – the ability of the brain to form new memories and learn new tasks. They found that two important indicators of brain function drastically improved in the mice with human glia. First, the researchers noted that the speed of wave transmission in the transplanted mice was faster than normally observed in mice, and more similar to that of human brain tissue. Second, the researchers looked at long-term potentiation (LTP), a process that measures how long the neurons in the brain are affected by a brief electrical stimulation. The researchers found that the transplanted mice developed more rapid and sustained LTP, suggesting an improved learning capability. When the team evaluated the mice in a series of behavioral tasks to test memory and learning ability, they found that the transplanted mice were more rapid learners and both acquired new associations and performed a variety of tasks significantly faster than mice without the human glial cells. More: • Mice Learn Faster with Human Glia • Mice get brain boost from transplanted human tissue • Human Brain Cells Boost Mouse Memory • Human Brain Cells Make Mice Smart • Mice Given Human Brain Cells Become Smarter • Human brain cells boost mouse memory • Glia brain cells: Not just infrastructure

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The normal development of an animal or plant can be compared with the successful performance of a symphony. The whole is the product of many events involving many different players; and these events must occur in an almost perfectly coordinated temporal and spatial sequence. In simple animals like the fruit fly and more recently in plants and mammals, some of the principal players in the developmental symphony have been identified. Now researchers have explained the operation of a mechanism in plants that controls a class of key developmental regulatory genes – homeobox genes. The homeobox genes under study (BREVIPEDICELLUS (BP) and KNAT2) need to be active in plant stem cells in order for the cells to maintain their non-specialized character. Stem cells are totipotent: they can differentiate, into any plant cell type, depending on signals they receive which send them down the developmental path. When the moment is just right for plant organs such as leaves to begin to grow, BP and KNAT2 are switched off so that development can proceed. “We were already familiar with the players in this regulatory mechanism, which have been conserved, or preserved, by evolution across species from flies to plants to animals,” says Marja Timmermans, who led the research team. “What we have not understood until now is how, in plants, the action of the players is very precisely coordinated in time and space.” It turns out that a highly conserved assembly of polycomb proteins – Polycomb-repressive complex2 (PRC2) – spurs epigenetic regulation that physically marks targeted genes, in this case, BP and KNAT2, for repression. But how do these protein complexes know where along the plant cell’s genome to go, and when, in order to induce this gene-repressing effect? The key discovery is the identification of the mechanism that brings PRC2 to specific sites along the genome precisely in those cells committed to become a leaf. Timmermans’ team showed that PRC2 physically interacts with DNA binding proteins that attach to plant DNA in specific genome regions just ahead of where the homeobox genes are situated. In the plant they studied, Arabidopsis, those DNA binding proteins are ASYMMETRIC LEAVES1 (AS1) and AS2. When a stem cell commits to becoming a leaf cell, AS1 and AS2 become active, attach at the DNA sites near BP and KNAT2, and recruit PRC2 to repress these homeobox genes. The epigenetic mark made by PRC2, which acts like a cellular memory, is heritable, and is essential in order for leaves and other plant organs to develop.

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With data from 73 ice and sediment core monitoring sites around the world, scientists have reconstructed Earth's temperature history back to the end of the last Ice Age. The analysis reveals that the planet today is warmer than it's been during 70% to 80% of the last 11,300 years. Lead paper author Shaun Marcott says that previous research on past global temperature change has largely focused on the last 2,000 years. Extending the reconstruction of global temperatures back to the end of the last Ice Age puts today's climate into a larger context. "We already knew that on a global scale, Earth is warmer today than it was over much of the past 2,000 years," Marcott says. "Now we know that it is warmer than most of the past 11,300 years." "The last century stands out as the anomaly in this record of global temperature since the end of the last ice age," says Candace Major, a program director in the National Science Foundation. "This research shows that we've experienced almost the same range of temperature change since the beginning of the industrial revolution," says Major, "as over the previous 11,000 years of Earth history – but this change happened a lot more quickly." What that history shows, the researchers say, is that during the last 5,000 years, the Earth on average cooled about 1.3 degrees Fahrenheit – until the last 100 years, when it warmed about 1.3 degrees F. Climate models project that global temperature will rise another 2.0 to 11.5 degrees F by the end of this century, largely dependent on the magnitude of carbon emissions. Of concern are projections of global temperature for the year 2100, when climate models evaluated by the Intergovernmental Panel on Climate Change show that temperatures will exceed the warmest temperatures during the 11,300-year period under all plausible greenhouse gas emission scenarios. "The Earth's climate is complex and responds to multiple forcings, including carbon dioxide and solar insolation," Marcott says. "Both changed very slowly over the past 11,000 years. But in the last 100 years, the increase in carbon dioxide through increased emissions from human activities has been significant. It's the only variable that can best explain the rapid increase in global temperatures." More: • True face of climate's hockey stick graph revealed • Global temperatures hung a U-turn in 1900, reversing a 5,000-year chill-down • Global temperatures are close to 11,000-year peak • Reconstruction of temperature history shows significance of recent warming

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A new experiment simulating conditions in deep space reveals that the complex building blocks of life could have been created on icy interplanetary dust and then carried to Earth, providing raw materials for the organic chemistry needed for life. The experimenters showed that conditions in space are capable of creating complex dipeptides – linked pairs of amino acids – that are essential building blocks shared by all living things. The discovery raises the possibility that these molecules were brought to Earth on a comet or possibly meteorites, catalyzing the formation of proteins (polypeptides), enzymes and even more complex molecules, such as sugars, that are necessary for life. While scientists have discovered basic organic molecules, such as amino acids, in numerous meteorites that have fallen to Earth, they have been unable to find the more complex molecular structures that are prerequisites for our planet’s biology. As a result, scientists have always assumed that the really complicated chemistry of life must have originated in Earth’s early oceans. In an ultra-high vacuum chamber chilled to 10 degrees above absolute zero (10 Kelvin), researchers simulated an icy snowball in space including carbon dioxide, ammonia and various hydrocarbons such as methane, ethane and propane. When zapped with high-energy electrons to simulate the cosmic rays in space, the chemicals reacted to form complex, organic compounds, specifically dipeptides. The organic residues were then analyzed with an instrument designed for ultrasensitive detection and identification of small organic molecules in the solar system. The analysis revealed the presence of complex molecules – nine different amino acids and at least two dipeptides – capable of catalyzing biological evolution on earth.

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Biologists have found that the removal of a genetic roadblock could improve the efficiency of converting adult cells into stem cells by 10 to 30 times. "The discovery six years ago that scientists can convert adult cells into inducible pluripotent stem cells, or iPSCs, bolstered the dream that a patient's own cells might be reprogrammed to make patient-specific iPSCs for regenerative medicine, modeling human diseases in petri dishes, and drug screening," said researcher Rongfu Wang. "But reprogramming efficiency has remained very low, impeding its applications in the clinic." Wang and his group identified a protein encoded by the gene Jmjd3 (also called KDM6B) as a roadblock in the stem cell conversion process. Jmjd3 is known to be involved in many biological processes, including the maturation of nerve cells and immune cell differentiation. Wang and his team found knockdown of Jmjd3 in young mouse fibroblasts was enough to greatly enhance reprogramming efficiency. "Our findings demonstrate a previously unrecognized role of Jmjd3 in cellular reprogramming and provide molecular insight into the mechanisms by which the Jmjd3-PHF20 axis controls this process," said Helen (Yicheng) Wang, co-principal investigator. In investigating Jmjd3 and its role in iPSC reprogramming, Wang's team found Jmjd3 has two previously unknown functions -- it helps regulate cell growth and cellular aging and it deactivates another nuclear protein, PHF20. The scientists learned during the study that PHF20 is required for cellular reprogramming, because cells without PHF20 failed to generate iPSCs.